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CD19 is widely expressed during all phases of B cell development until terminal differentiation into plasma cells. During B cell lymphopoiesis, CD19 surface expression starts during immunoglobulin (Ig) gene rearrangement, which coincides during B lineage commitment from hematopoietic stem cell. [8]
CD22, or cluster of differentiation-22, is a molecule belonging to the SIGLEC family of lectins. [4] It is found on the surface of mature B cells and to a lesser extent on some immature B cells. Generally speaking, CD22 is a regulatory molecule that prevents the overactivation of the immune system and the development of autoimmune diseases. [5]
B-cell-associated antigens such as CD19, CD20, CD22, and CD79a are usually expressed. In contrast to small lymphocytic lymphoma and mantle cell lymphoma (MCL), staining for CD5 is usually negative, and these lymphomas can be further distinguished with CD23 (positive in small lymphocytic lymphoma) and CyclinD1 (positive in MCL). [3]
Splenic B-cell lymphoma/leukemia unclassifiable: The rare reports on this lymphoma find the monoclonal B cells to be CD19+, CD20+ (bright, CD23+, CD11+, CD25−, CD103−, CD72+, and annexin A1−. [18] These cells, similar to the monoclonal cells in Hairy cell leukemia, [19] may have the V600E mutation in the BRAF gene. Patients with this ...
CD22 functions as an inhibitory receptor for B cell receptor (BCR) signalling. Like CD19, CD22 is a cell surface marker for lymphocytes that is present on most B cell malignancies, including acute lymphoblastic leukemia and various subtypes of non-Hodgkin lymphoma, including diffuse large B-cell lymphoma. CD22 expression has been shown to be ...
The tumor cells in Burkitt lymphoma generally strongly express markers of B cell differentiation (CD20, CD22, CD19), as well as CD10 and BCL6. The tumor cells are generally negative for BCL2 and TdT. The high mitotic activity of Burkitt lymphoma is confirmed by nearly 100% of the cells staining positive for Ki67. [23]
The CD nomenclature was proposed and established in the 1st International Workshop and Conference on Human Leukocyte Differentiation Antigens (HLDA), held in Paris in 1982. [4] [5] This system was intended for the classification of the many monoclonal antibodies (mAbs) generated by different laboratories around the world against epitopes on the surface molecules of leukocytes (white blood cells).
CD22: Walker & Smith conducted experiments with CD22 knock-outs and deletion mutants to discern CD22's function. [18] These mutant B cells did not infer any autoimmune disease, but they did see an increased production of autoantibodies due to the lack of BCR signalling inhibition, usually conducted by CD22. Autoantibodies are specific for self ...